Friday, December 23, 2011
Sunday, May 1, 2011
Steps toward a Bionic Eye
Artificial retinas that allow the blind to see
By Jamie Horder
Scientific American
February 15, 2011
The human eye is a biological marvel. Charles Darwin considered it one of the biggest challenges to his theory of evolution, famously writing: that “To suppose that the eye with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I freely confess, absurd in the highest degree.” Of course he did go on to explain how natural selection could account for the eye, but we can see why he wrote these words under the heading of “Organs of Extreme Perfection and Complication.”
The complexity and perfection of the eye has meant that, to date, it’s been all but impossible to reproduce its function artificially. Artificial hearts, kidneys (albeit outside the body), and ears ( cochlear implants) are all in widespread medical use -- but not eyes.
That might be about to change. In a remarkable achievement, a team of ophthalmologists and engineers has managed to partially restore vision to the blind, using an electronic device which acts as a replacement for the retina. The results are reported in a paper by Professor Eberhart Zrenner, Director of the Institute for Ophthalmic Research at the University Eye Hospital in Tuebingen, Germany.
The implant consists of a tiny panel, 3 by 3.1 mm in size, containing a 38 by 40 array of 1,500 light-sensitive microphotodiodes. These sensors detect light, and control the output of a pulsed electrical current. The brighter the light, the stronger the resulting current. Each sensor has its own microelectrode, and these are placed in contact with nerve cells in the retina, called bipolar cells, the first step on the pathway from the eye to the brain. The sensors therefore mimic the way the eye’s own photoreceptor cells normally function, turning light into a pattern of electrical impulses.
The implant is not a complete artificial eye. It relies on an intact eyeball, an intact retina with functioning bipolar cells, and an optic nerve to convey the information to the brain. This means that the technology is only useful in forms of blindness caused by selective damage to photoreceptor cells.
However, such blindness is unfortunately common. Retinitis pigmentosa is a disease that causes progressive loss of vision, as the photoreceptor cells degenerate, and eventually die. There are many different forms of the disorder, each caused by mutations in a different gene. In some people, the loss of vision is gradual, and they remain able to see for most of their lives. In others, it rapidly leads to blindness. It’s estimated that about 400,000 Americans suffer some form of the disease.
Zrenner and his team implanted their device in three patients, all of whom had been born with normal vision, but had become almost totally blind due to retinal degeneration. Two of them suffered from retinitis pigmentosa, while the third had a similar disease.
The surgical procedure was, naturally, delicate. It involved inserting a metal tube behind and into one of the patient’s eyes, through which the implant was put into place. The chip comes connected to a cable that provides it with power from an external battery. It also allows the patient to control the sensitivity of the electrodes – essentially, manually adjusting the “brightness” of the image, to compensate for changes in the overall level of light. This is something that the eye normally does so effortlessly that we’re rarely aware of it.
So what happened? All three patients regained vision to some extent. Patient 2, a 44 year old man with retinitis pigmentosa, experienced the most dramatic benefits. He began to lose his sight at the age of 16. The first problem he noticed was a difficulty seeing at night, a common early symptom. By the time of the study, he was virtually blind, although he could still tell the direction from which a light was shining.
Thanks to the implant, he gained the ability to recognize everyday objects including spoons, bananas, and apples; he could read a clock; and he could read letters, albeit slowly, and they had to be printed extremely large (about 5-8 cm high).
Videos of his abilities and his reactions to his newfound sight are available online.
This subretinal implant is not the only “bionic eye” idea under development, however. Other researchers have been working on using an external camera which transmits information to a relay chip placed on the retina, the "epiretinal” approach.
However, Zrenner’s team argues that their subretinal implant technique has some important advantages. Epiretinal devices have to pre-process the image before sending it to the retina, and patients need time to learn how to process the information that their brain receives, because the camera isn’t able to provide an exact simulation of normal retina outputs.
Zrenner et al’s subretinal method, however, took little “getting used to” because the implant is such a close analogue of the healthy retina. Also, they say that epiretinal approaches have so far only provided up to 60 pixels, as opposed to their 1,500.
Still, the technology has limitations. The image has no color, and it’s much less detailed than normal vision. The sensor has a resolution of 38 by 40 pixels, compared to the 960 by 640 resolution of an iPhone screen.
Being so small, it only covers a small fraction of the normal retinal field. However, this is actually less of a problem than it might first appear, because all of our detailed vision takes place in a tiny part of the retina, called the fovea. By placing the implant where the fovea used to be, the quality of the images was maximized.
The chip also requires an external power supply, so patients need to carry the battery pack and control unit around with them. Finally, they have a fairly hefty wire coming out of the side of their head.
So, at the moment, science is very far from being able to fully restore vision, but it’s still an exciting step forward. Technical improvements are sure to bring higher-quality images in the future.
Other researchers are working on using gene therapy to cure the underlying molecular cause of the disease, preventing the photoreceptors from dying in the first place. This approach has shown promise in animal models, and the results of the first human trials of gene therapy in another genetic eye disease, Leber’s ameurosis, have recently appeared.
So whether this device will become widely used in the treatment of people with diseases like retinitis pigmentosa is unclear. But it joins other emerging technologies, from deep brain stimulation to brain-computer interfaces, which are blurring the boundaries between the nervous system and machines.
Jamie Horder is a postdoctoral neuroscientist working at the Institute of Psychiatry in London. His current research focuses on autism.
By Jamie Horder
Scientific American
February 15, 2011
The human eye is a biological marvel. Charles Darwin considered it one of the biggest challenges to his theory of evolution, famously writing: that “To suppose that the eye with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I freely confess, absurd in the highest degree.” Of course he did go on to explain how natural selection could account for the eye, but we can see why he wrote these words under the heading of “Organs of Extreme Perfection and Complication.”
The complexity and perfection of the eye has meant that, to date, it’s been all but impossible to reproduce its function artificially. Artificial hearts, kidneys (albeit outside the body), and ears ( cochlear implants) are all in widespread medical use -- but not eyes.
That might be about to change. In a remarkable achievement, a team of ophthalmologists and engineers has managed to partially restore vision to the blind, using an electronic device which acts as a replacement for the retina. The results are reported in a paper by Professor Eberhart Zrenner, Director of the Institute for Ophthalmic Research at the University Eye Hospital in Tuebingen, Germany.
The implant consists of a tiny panel, 3 by 3.1 mm in size, containing a 38 by 40 array of 1,500 light-sensitive microphotodiodes. These sensors detect light, and control the output of a pulsed electrical current. The brighter the light, the stronger the resulting current. Each sensor has its own microelectrode, and these are placed in contact with nerve cells in the retina, called bipolar cells, the first step on the pathway from the eye to the brain. The sensors therefore mimic the way the eye’s own photoreceptor cells normally function, turning light into a pattern of electrical impulses.
The implant is not a complete artificial eye. It relies on an intact eyeball, an intact retina with functioning bipolar cells, and an optic nerve to convey the information to the brain. This means that the technology is only useful in forms of blindness caused by selective damage to photoreceptor cells.
However, such blindness is unfortunately common. Retinitis pigmentosa is a disease that causes progressive loss of vision, as the photoreceptor cells degenerate, and eventually die. There are many different forms of the disorder, each caused by mutations in a different gene. In some people, the loss of vision is gradual, and they remain able to see for most of their lives. In others, it rapidly leads to blindness. It’s estimated that about 400,000 Americans suffer some form of the disease.
Zrenner and his team implanted their device in three patients, all of whom had been born with normal vision, but had become almost totally blind due to retinal degeneration. Two of them suffered from retinitis pigmentosa, while the third had a similar disease.
The surgical procedure was, naturally, delicate. It involved inserting a metal tube behind and into one of the patient’s eyes, through which the implant was put into place. The chip comes connected to a cable that provides it with power from an external battery. It also allows the patient to control the sensitivity of the electrodes – essentially, manually adjusting the “brightness” of the image, to compensate for changes in the overall level of light. This is something that the eye normally does so effortlessly that we’re rarely aware of it.
So what happened? All three patients regained vision to some extent. Patient 2, a 44 year old man with retinitis pigmentosa, experienced the most dramatic benefits. He began to lose his sight at the age of 16. The first problem he noticed was a difficulty seeing at night, a common early symptom. By the time of the study, he was virtually blind, although he could still tell the direction from which a light was shining.
Thanks to the implant, he gained the ability to recognize everyday objects including spoons, bananas, and apples; he could read a clock; and he could read letters, albeit slowly, and they had to be printed extremely large (about 5-8 cm high).
Videos of his abilities and his reactions to his newfound sight are available online.
This subretinal implant is not the only “bionic eye” idea under development, however. Other researchers have been working on using an external camera which transmits information to a relay chip placed on the retina, the "epiretinal” approach.
However, Zrenner’s team argues that their subretinal implant technique has some important advantages. Epiretinal devices have to pre-process the image before sending it to the retina, and patients need time to learn how to process the information that their brain receives, because the camera isn’t able to provide an exact simulation of normal retina outputs.
Zrenner et al’s subretinal method, however, took little “getting used to” because the implant is such a close analogue of the healthy retina. Also, they say that epiretinal approaches have so far only provided up to 60 pixels, as opposed to their 1,500.
Still, the technology has limitations. The image has no color, and it’s much less detailed than normal vision. The sensor has a resolution of 38 by 40 pixels, compared to the 960 by 640 resolution of an iPhone screen.
Being so small, it only covers a small fraction of the normal retinal field. However, this is actually less of a problem than it might first appear, because all of our detailed vision takes place in a tiny part of the retina, called the fovea. By placing the implant where the fovea used to be, the quality of the images was maximized.
The chip also requires an external power supply, so patients need to carry the battery pack and control unit around with them. Finally, they have a fairly hefty wire coming out of the side of their head.
So, at the moment, science is very far from being able to fully restore vision, but it’s still an exciting step forward. Technical improvements are sure to bring higher-quality images in the future.
Other researchers are working on using gene therapy to cure the underlying molecular cause of the disease, preventing the photoreceptors from dying in the first place. This approach has shown promise in animal models, and the results of the first human trials of gene therapy in another genetic eye disease, Leber’s ameurosis, have recently appeared.
So whether this device will become widely used in the treatment of people with diseases like retinitis pigmentosa is unclear. But it joins other emerging technologies, from deep brain stimulation to brain-computer interfaces, which are blurring the boundaries between the nervous system and machines.
Jamie Horder is a postdoctoral neuroscientist working at the Institute of Psychiatry in London. His current research focuses on autism.
Tuesday, April 5, 2011
Neuro Myths: Separating Fact and Fiction in Brain-Based Learning
New research on educational neuroscience tells us how kids learn -- and how you should teach.
By Sara Bernard
Edutopia
December 1, 2010
You've surely heard the slogans: "Our educational games will give your brain a workout!" Or how about, "Give your students the cognitive muscles they need to build brain fitness." And then there's the program that "builds, enhances, and restores natural neural pathways to assist natural learning."
No one doubts that the brain is central to education, so the myriad products out there claiming to be based on research in neuroscience can look tempting.
With the great popularity of so-called brain-based learning, however, comes great risk. "So much of what is published and said is useless," says Kurt Fischer, founding president of the International Mind, Brain, and Education (MBE) Society and director of the MBE graduate program at Harvard University. "Much of it is wrong, a lot is empty or vapid, and some is not based in neuroscience at all."
Still, there are some powerful insights emerging from brain science that speak directly to how we teach in the classroom: learning experiences do help the brain grow, emotional safety does influence learning, and making lessons relevant can help information stick. The trick is separating the meat from the marketing.
So what's an educator to make of all these claims?
Standards of Proof
The use of neuroscience in education, relatively speaking, is young. Neuroimaging technologies have really only developed over the last 20 years, so virtually nothing is "proven" at this point. Neuroscientists can point to some aspects of how different parts of the brain function and connect with one another, but when it comes to education, no one can definitively outline more than a few broad concepts.
"My basic recommendation is that if a product claims to be proven by brain research, forget it," says neurologist and former classroom teacher Judy Willis. "Nothing from the lab can be proven to work in the classroom -- it can only correlate."
This might explain why some academics bemoan the term "brain-based learning," including Robert Sylwester, Emeritus Professor of Education at the University of Oregon. "As if it were kidney-based learning last year, and now it's brain based," he grumbles.
Some software companies will "make fabulous claims and have all these testimonials," adds Patricia Wolfe, veteran teacher and administrator and founder of Mind Matters, a workshop and online resource for translating brain science into classroom practice. But in many cases, she says, "the products haven't been tested by anyone who's not selling them."
Myth Busting
Some of the biggest neuro myths, or misguided beliefs about neuroscience that have invaded the general psyche, include the following:
• The brain is static, unchanging, and set before you start school. The most widely accepted conclusion of current research in neuroscience is that of neuroplasticity: Our brains grow, change, and adapt at all times in our lives. "Virtually everyone who studies the brain is astounded at how plastic it is," Fischer says.
• Some people are left-brained and some are right-brained. "This is total nonsense," says Fischer, "unless you've had half of your brain removed." This may have emerged from a misunderstanding of the split-brain work of Nobel Prize winner Roger Sperry, who noticed differences in the brain when he studied people whose left and right brains had been surgically disconnected.
• We use only 10 percent of our brains. This is also false, according to Wolfe, Fischer, and a slew of scientists across the globe. In fact, brain imaging has yet to produce evidence of any inactive areas in a healthy brain.
• Male and female brains are radically different. Though there may be subtle differences between male and female brains, there is absolutely no significant evidence to suggest that the genders learn or should be taught differently. This myth might stem from a misinterpretation of books such as The Essential Difference: Men, Women, and the Extreme Male Brain, which focused largely on patients with autism.
• The ages 0-3 are more important than any other age for learning. Even though the connections between neurons, called synapses, are greatest in number during this period, many of the published studies that have to do with teaching during these "critical" time periods involved rats and mazes, not human beings.
"Understanding the Brain: The Birth of a Learning Science," a report published by the Organisation for Economic Co-Operation and Development (OECD), examines these and other unfounded neuroscience claims. Unfortunately, the science behind these ideas is often misunderstood and milked for profit.
Use What Works
Consider the case of Fast ForWord, the much-lauded phonics-based reading software, which is listed on the U.S. Department of Education's What Works Clearinghouse as demonstrating "potentially positive effects on the reading fluency and comprehension domains for adolescent learners." A 2008 study published in the Journal of Speech, Language, and Hearing Research, however, reported that the software "was not more effective at improving general language skills or temporal processing skills than a nonspecific comparison treatment."
Some neuroscientists maintain that Fast ForWord is a prime example of what happens in the brain-based education industry: A few limited studies with a neuroscientific basis are used to underscore decades of marketing. Yet many schools and teachers across the nation who've used Fast ForWord have seen astronomical gains in their students' reading capabilities.
In other words, the conclusions here are murky at best. If a strategy or program produces results, use it. Just don't assume that its value is unequivocally proven by brain science.
We don't need to be so wary of discoveries in neuroscience that we write them off, however. They can still contribute enormously to a dynamic classroom, especially if they're seen as a "tool, rather than a philosophy," as one educator, LoriC, put it in an Edutopia.org discussion. (For specific strategies, see the "Fact" links at right.) "Maybe we need to approach this sort of learning like Thomas Edison might have," she wrote. "Try it, see what works, and learn as much from the failures as you do from the successes."
Plus, neuroscientists urge educators to trust themselves on this. If a claim seems off, it probably is, and if it confirms something that already seems to work, it's probably on the right track. "Usually, when scientists discover something true about the brain," notes Sylwester, "it doesn't surprise teachers."
By Sara Bernard
Edutopia
December 1, 2010
You've surely heard the slogans: "Our educational games will give your brain a workout!" Or how about, "Give your students the cognitive muscles they need to build brain fitness." And then there's the program that "builds, enhances, and restores natural neural pathways to assist natural learning."
No one doubts that the brain is central to education, so the myriad products out there claiming to be based on research in neuroscience can look tempting.
With the great popularity of so-called brain-based learning, however, comes great risk. "So much of what is published and said is useless," says Kurt Fischer, founding president of the International Mind, Brain, and Education (MBE) Society and director of the MBE graduate program at Harvard University. "Much of it is wrong, a lot is empty or vapid, and some is not based in neuroscience at all."
Still, there are some powerful insights emerging from brain science that speak directly to how we teach in the classroom: learning experiences do help the brain grow, emotional safety does influence learning, and making lessons relevant can help information stick. The trick is separating the meat from the marketing.
So what's an educator to make of all these claims?
Standards of Proof
The use of neuroscience in education, relatively speaking, is young. Neuroimaging technologies have really only developed over the last 20 years, so virtually nothing is "proven" at this point. Neuroscientists can point to some aspects of how different parts of the brain function and connect with one another, but when it comes to education, no one can definitively outline more than a few broad concepts.
"My basic recommendation is that if a product claims to be proven by brain research, forget it," says neurologist and former classroom teacher Judy Willis. "Nothing from the lab can be proven to work in the classroom -- it can only correlate."
This might explain why some academics bemoan the term "brain-based learning," including Robert Sylwester, Emeritus Professor of Education at the University of Oregon. "As if it were kidney-based learning last year, and now it's brain based," he grumbles.
Some software companies will "make fabulous claims and have all these testimonials," adds Patricia Wolfe, veteran teacher and administrator and founder of Mind Matters, a workshop and online resource for translating brain science into classroom practice. But in many cases, she says, "the products haven't been tested by anyone who's not selling them."
Myth Busting
Some of the biggest neuro myths, or misguided beliefs about neuroscience that have invaded the general psyche, include the following:
• The brain is static, unchanging, and set before you start school. The most widely accepted conclusion of current research in neuroscience is that of neuroplasticity: Our brains grow, change, and adapt at all times in our lives. "Virtually everyone who studies the brain is astounded at how plastic it is," Fischer says.
• Some people are left-brained and some are right-brained. "This is total nonsense," says Fischer, "unless you've had half of your brain removed." This may have emerged from a misunderstanding of the split-brain work of Nobel Prize winner Roger Sperry, who noticed differences in the brain when he studied people whose left and right brains had been surgically disconnected.
• We use only 10 percent of our brains. This is also false, according to Wolfe, Fischer, and a slew of scientists across the globe. In fact, brain imaging has yet to produce evidence of any inactive areas in a healthy brain.
• Male and female brains are radically different. Though there may be subtle differences between male and female brains, there is absolutely no significant evidence to suggest that the genders learn or should be taught differently. This myth might stem from a misinterpretation of books such as The Essential Difference: Men, Women, and the Extreme Male Brain, which focused largely on patients with autism.
• The ages 0-3 are more important than any other age for learning. Even though the connections between neurons, called synapses, are greatest in number during this period, many of the published studies that have to do with teaching during these "critical" time periods involved rats and mazes, not human beings.
"Understanding the Brain: The Birth of a Learning Science," a report published by the Organisation for Economic Co-Operation and Development (OECD), examines these and other unfounded neuroscience claims. Unfortunately, the science behind these ideas is often misunderstood and milked for profit.
Use What Works
Consider the case of Fast ForWord, the much-lauded phonics-based reading software, which is listed on the U.S. Department of Education's What Works Clearinghouse as demonstrating "potentially positive effects on the reading fluency and comprehension domains for adolescent learners." A 2008 study published in the Journal of Speech, Language, and Hearing Research, however, reported that the software "was not more effective at improving general language skills or temporal processing skills than a nonspecific comparison treatment."
Some neuroscientists maintain that Fast ForWord is a prime example of what happens in the brain-based education industry: A few limited studies with a neuroscientific basis are used to underscore decades of marketing. Yet many schools and teachers across the nation who've used Fast ForWord have seen astronomical gains in their students' reading capabilities.
In other words, the conclusions here are murky at best. If a strategy or program produces results, use it. Just don't assume that its value is unequivocally proven by brain science.
We don't need to be so wary of discoveries in neuroscience that we write them off, however. They can still contribute enormously to a dynamic classroom, especially if they're seen as a "tool, rather than a philosophy," as one educator, LoriC, put it in an Edutopia.org discussion. (For specific strategies, see the "Fact" links at right.) "Maybe we need to approach this sort of learning like Thomas Edison might have," she wrote. "Try it, see what works, and learn as much from the failures as you do from the successes."
Plus, neuroscientists urge educators to trust themselves on this. If a claim seems off, it probably is, and if it confirms something that already seems to work, it's probably on the right track. "Usually, when scientists discover something true about the brain," notes Sylwester, "it doesn't surprise teachers."
Thursday, February 10, 2011
Multiple Intelligences
Taken from the webpage of
Dr. Thomas Armstrong
The theory of multiple intelligences was developed in 1983 by Dr. Howard Gardner, professor of education at Harvard University. It suggests that the traditional notion of intelligence, based on I.Q. testing, is far too limited. Instead, Dr. Gardner proposes eight different intelligences to account for a broader range of human potential in children and adults. These intelligences are:
•Linguistic intelligence ("word smart")
•Logical-mathematical intelligence ("number/reasoning smart")
•Spatial intelligence ("picture smart")
•Bodily-Kinesthetic intelligence ("body smart")
•Musical intelligence ("music smart")
•Interpersonal intelligence ("people smart")
•Intrapersonal intelligence ("self smart")
•Naturalist intelligence ("nature smart")
Dr. Gardner says that our schools and culture focus most of their attention on linguistic and logical-mathematical intelligence. We esteem the highly articulate or logical people of our culture. However, Dr. Gardner says that we should also place equal attention on individuals who show gifts in the other intelligences: the artists, architects, musicians, naturalists, designers, dancers, therapists, entrepreneurs, and others who enrich the world in which we live. Unfortunately, many children who have these gifts don’t receive much reinforcement for them in school. Many of these kids, in fact, end up being labeled "learning disabled," "ADD (attention deficit disorder," or simply underachievers, when their unique ways of thinking and learning aren’t addressed by a heavily linguistic or logical-mathematical classroom. The theory of multiple intelligences proposes a major transformation in the way our schools are run. It suggests that teachers be trained to present their lessons in a wide variety of ways using music, cooperative learning, art activities, role play, multimedia, field trips, inner reflection, and much more (see Multiple Intelligences in the Classroom). The good news is that the theory of multiple intelligences has grabbed the attention of many educators around the country, and hundreds of schools are currently using its philosophy to redesign the way it educates children. The bad news is that there are thousands of schools still out there that teach in the same old dull way, through dry lectures, and boring worksheets and textbooks. The challenge is to get this information out to many more teachers, school administrators, and others who work with children, so that each child has the opportunity to learn in ways harmonious with their unique minds (see In Their Own Way).
The theory of multiple intelligences also has strong implications for adult learning and development. Many adults find themselves in jobs that do not make optimal use of their most highly developed intelligences (for example, the highly bodily-kinesthetic individual who is stuck in a linguistic or logical desk-job when he or she would be much happier in a job where they could move around, such as a recreational leader, a forest ranger, or physical therapist). The theory of multiple intelligences gives adults a whole new way to look at their lives, examining potentials that they left behind in their childhood (such as a love for art or drama) but now have the opportunity to develop through courses, hobbies, or other programs of self-development (see 7 Kinds of Smart).
How to Teach or Learn Anything 8 Different Ways
One of the most remarkable features of the theory of multiple intelligences is how it provides eight different potential pathways to learning. If a teacher is having difficulty reaching a student in the more traditional linguistic or logical ways of instruction, the theory of multiple intelligences suggests several other ways in which the material might be presented to facilitate effective learning. Whether you are a kindergarten teacher, a graduate school instructor, or an adult learner seeking better ways of pursuing self-study on any subject of interest, the same basic guidelines apply. Whatever you are teaching or learning, see how you might connect it with
•words (linguistic intelligence)
•numbers or logic (logical-mathematical intelligence)
•pictures (spatial intelligence)
•music (musical intelligence)
•self-reflection (intrapersonal intelligence)
•a physical experience (bodily-kinesthetic intelligence)
•a social experience (interpersonal intelligence), and/or
•an experience in the natural world. (naturalist intelligence)
For example, if you’re teaching or learning about the law of supply and demand in economics, you might read about it (linguistic), study mathematical formulas that express it (logical-mathematical), examine a graphic chart that illustrates the principle (spatial), observe the law in the natural world (naturalist) or in the human world of commerce (interpersonal); examine the law in terms of your own body [e.g. when you supply your body with lots of food, the hunger demand goes down; when there's very little supply, your stomach's demand for food goes way up and you get hungry] (bodily-kinesthetic and intrapersonal); and/or write a song (or find an existing song) that demonstrates the law (perhaps Dylan's "Too Much of Nothing?").
You don’t have to teach or learn something in all eight ways, just see what the possibilities are, and then decide which particular pathways interest you the most, or seem to be the most effective teaching or learning tools. The theory of multiple intelligences is so intriguing because it expands our horizon of available teaching/learning tools beyond the conventional linguistic and logical methods used in most schools (e.g. lecture, textbooks, writing assignments, formulas, etc.). To get started, put the topic of whatever you’re interested in teaching or learning about in the center of a blank sheet of paper, and draw eight straight lines or "spokes" radiating out from this topic. Label each line with a different intelligence. Then start brainstorming ideas for teaching or learning that topic and write down ideas next to each intelligence (this is a spatial-linguistic approach of brainstorming; you might want to do this in other ways as well, using a tape-recorder, having a group brainstorming session, etc.). Have fun!
Dr. Thomas Armstrong
The theory of multiple intelligences was developed in 1983 by Dr. Howard Gardner, professor of education at Harvard University. It suggests that the traditional notion of intelligence, based on I.Q. testing, is far too limited. Instead, Dr. Gardner proposes eight different intelligences to account for a broader range of human potential in children and adults. These intelligences are:
•Linguistic intelligence ("word smart")
•Logical-mathematical intelligence ("number/reasoning smart")
•Spatial intelligence ("picture smart")
•Bodily-Kinesthetic intelligence ("body smart")
•Musical intelligence ("music smart")
•Interpersonal intelligence ("people smart")
•Intrapersonal intelligence ("self smart")
•Naturalist intelligence ("nature smart")
Dr. Gardner says that our schools and culture focus most of their attention on linguistic and logical-mathematical intelligence. We esteem the highly articulate or logical people of our culture. However, Dr. Gardner says that we should also place equal attention on individuals who show gifts in the other intelligences: the artists, architects, musicians, naturalists, designers, dancers, therapists, entrepreneurs, and others who enrich the world in which we live. Unfortunately, many children who have these gifts don’t receive much reinforcement for them in school. Many of these kids, in fact, end up being labeled "learning disabled," "ADD (attention deficit disorder," or simply underachievers, when their unique ways of thinking and learning aren’t addressed by a heavily linguistic or logical-mathematical classroom. The theory of multiple intelligences proposes a major transformation in the way our schools are run. It suggests that teachers be trained to present their lessons in a wide variety of ways using music, cooperative learning, art activities, role play, multimedia, field trips, inner reflection, and much more (see Multiple Intelligences in the Classroom). The good news is that the theory of multiple intelligences has grabbed the attention of many educators around the country, and hundreds of schools are currently using its philosophy to redesign the way it educates children. The bad news is that there are thousands of schools still out there that teach in the same old dull way, through dry lectures, and boring worksheets and textbooks. The challenge is to get this information out to many more teachers, school administrators, and others who work with children, so that each child has the opportunity to learn in ways harmonious with their unique minds (see In Their Own Way).
The theory of multiple intelligences also has strong implications for adult learning and development. Many adults find themselves in jobs that do not make optimal use of their most highly developed intelligences (for example, the highly bodily-kinesthetic individual who is stuck in a linguistic or logical desk-job when he or she would be much happier in a job where they could move around, such as a recreational leader, a forest ranger, or physical therapist). The theory of multiple intelligences gives adults a whole new way to look at their lives, examining potentials that they left behind in their childhood (such as a love for art or drama) but now have the opportunity to develop through courses, hobbies, or other programs of self-development (see 7 Kinds of Smart).
How to Teach or Learn Anything 8 Different Ways
One of the most remarkable features of the theory of multiple intelligences is how it provides eight different potential pathways to learning. If a teacher is having difficulty reaching a student in the more traditional linguistic or logical ways of instruction, the theory of multiple intelligences suggests several other ways in which the material might be presented to facilitate effective learning. Whether you are a kindergarten teacher, a graduate school instructor, or an adult learner seeking better ways of pursuing self-study on any subject of interest, the same basic guidelines apply. Whatever you are teaching or learning, see how you might connect it with
•words (linguistic intelligence)
•numbers or logic (logical-mathematical intelligence)
•pictures (spatial intelligence)
•music (musical intelligence)
•self-reflection (intrapersonal intelligence)
•a physical experience (bodily-kinesthetic intelligence)
•a social experience (interpersonal intelligence), and/or
•an experience in the natural world. (naturalist intelligence)
For example, if you’re teaching or learning about the law of supply and demand in economics, you might read about it (linguistic), study mathematical formulas that express it (logical-mathematical), examine a graphic chart that illustrates the principle (spatial), observe the law in the natural world (naturalist) or in the human world of commerce (interpersonal); examine the law in terms of your own body [e.g. when you supply your body with lots of food, the hunger demand goes down; when there's very little supply, your stomach's demand for food goes way up and you get hungry] (bodily-kinesthetic and intrapersonal); and/or write a song (or find an existing song) that demonstrates the law (perhaps Dylan's "Too Much of Nothing?").
You don’t have to teach or learn something in all eight ways, just see what the possibilities are, and then decide which particular pathways interest you the most, or seem to be the most effective teaching or learning tools. The theory of multiple intelligences is so intriguing because it expands our horizon of available teaching/learning tools beyond the conventional linguistic and logical methods used in most schools (e.g. lecture, textbooks, writing assignments, formulas, etc.). To get started, put the topic of whatever you’re interested in teaching or learning about in the center of a blank sheet of paper, and draw eight straight lines or "spokes" radiating out from this topic. Label each line with a different intelligence. Then start brainstorming ideas for teaching or learning that topic and write down ideas next to each intelligence (this is a spatial-linguistic approach of brainstorming; you might want to do this in other ways as well, using a tape-recorder, having a group brainstorming session, etc.). Have fun!
Monday, February 7, 2011
Testing Autism Drugs in Human Brain Cells
A Method Involving Pluripotent Stem Cells Could Lead to Personalized Treatment of the Disease
By Jennifer Chu
Technology Review
November 11, 2010
Autism is a highly complex disorder affecting one in every 110 children born in the United States. The disease's genetic profile and behavioral symptoms fluctuate widely from case to case, and this variability has frustrated scientists' efforts to identify effective treatments. A new study suggests that autism could eventually be a target for personalized treatment, targeted to a patient's own neurons.
A team from the University of California, San Diego, and the Salk Institute for Biological Studies devised a way to study brain cells from patients with autism, and found a way reverse cellular abnormalities in neurons that have been associated with autism.
The researchers took skin biopsies from patients with a severe form of autism called Rett syndrome, and genetically reprogrammed those cells into pluripotent stem cells. Pluripotent stem cells have the power to differentiate into any kind of cell in the body, depending on environmental cues during early development. The team differentiated the stem cells into fully functioning neurons, and then studied their functioning. They found that neurons derived from patients with Rett syndrome showed certain abnormalities, including markedly smaller cell bodies, dendrite connections, and decreased cell-to-cell communication.
By treating these patient-derived neurons with an experimental drug, the researchers could reverse the cellular abnormalities. The findings, published today in the journal Cell, could give scientists a powerful tool for pinpointing the causes of autism and other brain disorders, and a way to choose targeted treatments.
"It took us two years to finish this project, and personalized medicine might not be that far off," says Carol Marchetto, first author of the paper and a postdoctoral researcher at the Salk Institute. "In the lifetime of a patient, you could go from his skin sample to a reprogrammed cell, to differentiating into a neuron, and find drugs that could be used on that patient."
Rett syndrome, which mostly affects girls, can cause highly impaired social and communication skills, which become apparent soon after a child learns to walk and talk. Patients with Rett can experience increased difficulty breathing and controlling their movements, and can develop repetitive and compulsive behaviors similar to other forms of autism.
Marchetto sees Rett syndrome as a gateway to the broader study of autism, since many other forms of autism share behavioral and genetic similarities with Rett syndrome.
Most cases of autism seem to stem from a combination of genetic abnormalities, but Rett arises from a single gene mutation, found on the MeCP2 gene on the X chromosome. In girls, one of two X chromosomes carries the mutation, and during fetal brain development, one chromosome is activated within each brain cell, seemingly at random. Rett patients can exhibit varying percentages of brain cells carrying the mutation, which can manifest as varying levels of severity of the disorder.
To understand how this genetic mutation plays out at a cellular level, Marchetto and her colleague Alysson Muotri, an assistant professor in the department of Molecular and Cellular Medicine at the UCSD's School of Medicine, took skin biopsies from four patients with Rett syndrome, reprogrammed them into pluripotent stem cells and experimented with a number of different conditions before they found a combination of growth factors that differentiated the stem cells into functioning human neurons.
They saw that each patient-derived stem-cell line generated a different percentage of neurons carrying the gene mutation. The defective neurons looked and acted differently from their normal counterparts, exhibiting smaller cell bodies, less dendrite connections, and impaired cell-to-cell communication.
The researchers treated neuron cultures with insulin-like growth factor (iGF1), which has been shown to reverse behavioral symptoms of Rett in mice. The drug reversed the biological symptoms of the disorder in the neurons, restoring dendrite connections and cell-to-cell signaling in defective neurons. The researchers plan to use the same process to generate neurons from more patients with both Rett syndrome and other forms of autism.
Jeffrey Neul, assistant professor of molecular and human genetics at Baylor College of Medicine, who studies Rett syndrome in mice, says animal models allow scientists to observe the behavioral effects of the disease, but this is a time- and labor-intensive process.
"The field really has been in desperate need of cellular-based assays that can be used to test therapeutic compounds," says Neul. "And it's really hard to push drug discovery if you don't have something you can do in a more rapid fashion."
The process Marchetto and Muotri have developed takes three months to generate fully functioning human neurons. While this is similar to the time frame of normal brain development, the researchers are looking for ways to speed the process up so they can rapidly generate brain cells and expose them to a variety of molecular factors and drug compounds.
The team also plans to move beyond the Petri dish once they've differentiated neurons from human skin cells, to see how the neurons work in a living brain. "What we can do is transplant human neurons in mouse brains and generate chimeric [hybrid human-animal] models," says Muotri. "We can then expose these animals to different environments, and see how they will affect the human neuron."
James Ellis, professor of molecular genetics at the University of Toronto, is doing similar work in reprogramming patients' skin cells into brain cells. He says that Muotri and Marchetto's findings open up a new testing ground for autism and other neurological disorders. "That's clearly what's going to be required of autism, where different people are going to have different mutations and mechanisms, in how they ended up with that outcome," he says.
By Jennifer Chu
Technology Review
November 11, 2010
Autism is a highly complex disorder affecting one in every 110 children born in the United States. The disease's genetic profile and behavioral symptoms fluctuate widely from case to case, and this variability has frustrated scientists' efforts to identify effective treatments. A new study suggests that autism could eventually be a target for personalized treatment, targeted to a patient's own neurons.
A team from the University of California, San Diego, and the Salk Institute for Biological Studies devised a way to study brain cells from patients with autism, and found a way reverse cellular abnormalities in neurons that have been associated with autism.
The researchers took skin biopsies from patients with a severe form of autism called Rett syndrome, and genetically reprogrammed those cells into pluripotent stem cells. Pluripotent stem cells have the power to differentiate into any kind of cell in the body, depending on environmental cues during early development. The team differentiated the stem cells into fully functioning neurons, and then studied their functioning. They found that neurons derived from patients with Rett syndrome showed certain abnormalities, including markedly smaller cell bodies, dendrite connections, and decreased cell-to-cell communication.
By treating these patient-derived neurons with an experimental drug, the researchers could reverse the cellular abnormalities. The findings, published today in the journal Cell, could give scientists a powerful tool for pinpointing the causes of autism and other brain disorders, and a way to choose targeted treatments.
"It took us two years to finish this project, and personalized medicine might not be that far off," says Carol Marchetto, first author of the paper and a postdoctoral researcher at the Salk Institute. "In the lifetime of a patient, you could go from his skin sample to a reprogrammed cell, to differentiating into a neuron, and find drugs that could be used on that patient."
Rett syndrome, which mostly affects girls, can cause highly impaired social and communication skills, which become apparent soon after a child learns to walk and talk. Patients with Rett can experience increased difficulty breathing and controlling their movements, and can develop repetitive and compulsive behaviors similar to other forms of autism.
Marchetto sees Rett syndrome as a gateway to the broader study of autism, since many other forms of autism share behavioral and genetic similarities with Rett syndrome.
Most cases of autism seem to stem from a combination of genetic abnormalities, but Rett arises from a single gene mutation, found on the MeCP2 gene on the X chromosome. In girls, one of two X chromosomes carries the mutation, and during fetal brain development, one chromosome is activated within each brain cell, seemingly at random. Rett patients can exhibit varying percentages of brain cells carrying the mutation, which can manifest as varying levels of severity of the disorder.
To understand how this genetic mutation plays out at a cellular level, Marchetto and her colleague Alysson Muotri, an assistant professor in the department of Molecular and Cellular Medicine at the UCSD's School of Medicine, took skin biopsies from four patients with Rett syndrome, reprogrammed them into pluripotent stem cells and experimented with a number of different conditions before they found a combination of growth factors that differentiated the stem cells into functioning human neurons.
They saw that each patient-derived stem-cell line generated a different percentage of neurons carrying the gene mutation. The defective neurons looked and acted differently from their normal counterparts, exhibiting smaller cell bodies, less dendrite connections, and impaired cell-to-cell communication.
The researchers treated neuron cultures with insulin-like growth factor (iGF1), which has been shown to reverse behavioral symptoms of Rett in mice. The drug reversed the biological symptoms of the disorder in the neurons, restoring dendrite connections and cell-to-cell signaling in defective neurons. The researchers plan to use the same process to generate neurons from more patients with both Rett syndrome and other forms of autism.
Jeffrey Neul, assistant professor of molecular and human genetics at Baylor College of Medicine, who studies Rett syndrome in mice, says animal models allow scientists to observe the behavioral effects of the disease, but this is a time- and labor-intensive process.
"The field really has been in desperate need of cellular-based assays that can be used to test therapeutic compounds," says Neul. "And it's really hard to push drug discovery if you don't have something you can do in a more rapid fashion."
The process Marchetto and Muotri have developed takes three months to generate fully functioning human neurons. While this is similar to the time frame of normal brain development, the researchers are looking for ways to speed the process up so they can rapidly generate brain cells and expose them to a variety of molecular factors and drug compounds.
The team also plans to move beyond the Petri dish once they've differentiated neurons from human skin cells, to see how the neurons work in a living brain. "What we can do is transplant human neurons in mouse brains and generate chimeric [hybrid human-animal] models," says Muotri. "We can then expose these animals to different environments, and see how they will affect the human neuron."
James Ellis, professor of molecular genetics at the University of Toronto, is doing similar work in reprogramming patients' skin cells into brain cells. He says that Muotri and Marchetto's findings open up a new testing ground for autism and other neurological disorders. "That's clearly what's going to be required of autism, where different people are going to have different mutations and mechanisms, in how they ended up with that outcome," he says.
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